Hallucinogenic Mushroom Toxicity 

Updated: Jul 06, 2017
Author: Louis Rolston-Cregler, MD; Chief Editor: Sage W Wiener, MD 

Overview

Practice Essentials

For the most part, mushrooms with significant psychoactive effects fall into the following 2 groups[1] :

  • Mushrooms containing ibotenic acid and muscimol (isoxazoles) – Amanita gemmata, Amanita muscaria (also called fly agaric or soma), and Amanita pantherina (also called panther or panther amanita); these are not to be confused with the deadly Amanita phalloides, Amanita verna, and Amanita virosa.

  • Mushrooms containing psilocybin – Psilocybe caerulipes, Psilocybe cubensis, Gymnopilus spectabilis, Panaeolus species (eg, Panaeolus foenisecii), and Psathyrella foenisecii

 

The timing of symptom onset is important for distinguishing life-threatening or severe mushroom poisonings from less serious poisonings (eg, those involving hallucinogenic mushrooms), which typically have an onset of symptoms well within 5 hours of ingestion. If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 hours or more after ingestion, mushrooms that can cause potentially life-threatening or severe toxicity (eg, A phalloides or Cortinarius spp) should be considered (see Presentation).

No particular diagnostic procedures are available or needed for most patients. Laboratory studies can be helpful in identifying complications of hallucinogenic mushroom abuse. Identification of the mushroom by a mycologist is desirable (see Workup).

Care is primarily supportive. Symptoms usually subside in 6-8 hours, though some may take as long as several days to resolve fully. Benzodiazepines may be used for sedation and treatment of panic attacks, hallucinations, and seizures. Psychiatric consultation and evaluation may be needed in some cases (see Treatment).

For patient education resources, see the Poisoning - First Aid and Emergency Center, as well as Poisoning and Activated Charcoal.

 

Background

Hallucinogenic mushroom toxicity is not a new phenomenon: Hallucinogenic fungi have been used in divinatory or religious contexts for at least 3000 years. However, it was not until the 1950s that the involved species of fungi were identified and the chemical nature of the active substances was determined.[2]

Consumption of hallucinogenic mushrooms continues to be popular today in some settings. Motives for their use include simple experimentation; a desire to enhance routine experiences, emotions, or social interactions; to disconnect from reality; to induce visions; as a psychotherapeutic tool; or for mystical or spiritual reasons.[3]

For centuries, Amanita muscaria has been consumed in central Asia as a hallucinogen. Some Siberian tribes report that 3 fresh A muscaria mushrooms can be lethal, whereas others claim that eating as many as 21 of these mushrooms is safe. Various hallucinogenic mushrooms containing ibotenic acid and muscimol or psilocybin are found in the New World. Reports of toxicity associated with this group of mushrooms have increased as a consequence of their growing popularity as hallucinogens.[4]

Pathophysiology

A muscaria,A pantherina, and A gemmata contain ibotenic acid, muscimol, and muscazone. These isoxazole derivatives are present in various concentrations, depending on environmental conditions, the maturity of the fungus, and the season of the year. Ibotenic acid and muscimol are relatively stable: Toxic activity has been maintained in dried plants for as long as 7 years.

Other toxins are probably present in these mushrooms; pure extracts of ibotenic acid or muscimol do not reproduce all of the symptoms observed after their ingestion. Although muscarinic acid originally was isolated from A muscaria, as the name suggests, muscarine does not appear to be of particular clinical significance in A muscaria poisoning; in fact, anticholinergic findings may be observed in this setting. A muscaria also lacks the amatoxins seen in other Amanita species.

Ibotenic acid resembles glutamic acid and is an agonist at central glutamic acid receptors; its decarboxylated derivative, muscimol, is an agonist at gamma-aminobutyric acid (GABA) receptors. The central effects of these hallucinogenic mushrooms are thought to be attributable to these actions.[2] Both ibotenic acid and muscimol can cross the blood-brain barrier.[5]

Many of the central nervous system (CNS) effects of muscimol (eg, sedation) are ascribed to its ability to act as a GABA agonist. By comparison, ibotenic acid is more of a CNS stimulant, by virtue of its action on glutamic acid receptors. In humans, most of the ibotenic acid ingested is excreted unchanged in the urine, with only some of it being metabolized to muscimol. About one third of the muscimol ingested is excreted unchanged, another third is conjugated, and the remaining third is oxidized.[5]

The Psilocybe, Gymnopilus, Panaeolus, and Psathyrella species previously mentioned (see Background) contain the indoles psilocybin and psilocin. Psilocin and its phosphate ester, psilocybin, are similar in structure to lysergic acid diethylamide (LSD). They are structural analogues of serotonin (5-hydroxytryptamine [5-HT]); thus, hallucinogenic effects probably are mediated through effects on serotonergic receptors.[2]

Etiology

Hallucinogenic mushroom toxicity is caused by ingestion of fungi containing ibotenic acid, muscimol, psilocybin, or psilocin. Circumstances that could lead to such ingestion include the following:

  • Adults and adolescents seeking to achieve a state of intoxication – This is the most common reason for ingesting these mushrooms[1]

  • Incorrect mushroom identification by a naive forager (eg, a novice mushroom harvester or an immigrant who mistakes a local poisonous variety for an edible variety native to his or her homeland)

  • Intentional ingestion by a suicidal person

  • Unintentional ingestion by a child who found mushrooms growing in yards or outdoor play areas

  • Foul play, in which an individual is poisoned by someone else

  • Inadvertent poisoning from dried mushrooms purchased on the Internet or from other sources where the composition of the mushroom is unreliable or where the mushroom might be contaminated with unknown toxic compounds

Epidemiology

United States statistics

Determination of the frequency of hallucinogenic mushroom toxicity is limited by the lack of a national reporting system or registry for mushroom poisoning and by the likelihood that many affected individuals may never seek medical attention. However, estimates based on small studies or surveillance systems using self-reporting are available.

In a study of 174 adolescents with a history of substance abuse, 45 (26%) reported having used hallucinogenic mushrooms at some point in their life, often in combination with alcohol or marijuana.[6]

On the basis of data collected from September 2008 to December 2009, the Youth Risk Behavior Surveillance System reported that 8% of students had used a hallucinogenic drug (eg, LSD, phencyclidine [PCP; angel dust], mescaline, or mushrooms) at least once in their life.[7] Hallucinogen use was more common among males and whites than among females and African Americans and Hispanics.

In 2015, 6091 mushroom ingestions were reported to the National Poison Data System of the American Association of Poison Control Centers (AAPCC) resulting in a single death. Mushrooms of unknown type were involved in 85% of reported ingestions. involved. Mushrooms containing psilocybin and psilocin accounted for 473 cases, with 311 involving single-substance exposures; 16 (5%) of the 311 involved children younger than 6 years. About 85% of all cases of psilocybin and psilocin mushroom poisoning resulted from intentional ingestion, and 76% were treated at a healthcare facility.[8]

Age-related demographics

Few data exist on the age distribution of hallucinogenic mushroom users; however, some general observations may be made.

Adults are frequently involved as foragers for edible mushrooms; because of errors in identification, they may ingest toxin-containing lookalike mushrooms. Adults and adolescents may also be poisoned when they intentionally consume mushrooms, picked from the ground or purchased dried, to achieve intoxication. In particular, college students are known to abuse psilocybin mushrooms.[9, 10, 11]

Young children may experience mushroom poisoning when they eat mushrooms found outside, typically in yards or outdoor play areas. Reports of seizurelike activity have been reported for children but are not typical in adults.[12, 13]

Prognosis

Use of hallucinogenic mushrooms rarely results in life-threatening symptoms.[14] The prognosis is generally excellent. Many patients who ingest these mushrooms exhibit only minor symptoms or no symptoms at all. Symptoms typically are mild to moderate in severity and self-limited, though some effects of ibotenic acid poisoning, particularly headache, may take 2 days or more to resolve.[12, 13] Patients commonly recover without drug therapy. Fatalities from hallucinogenic mushroom poisoning are rare.

From 1999 to 2009, 35 deaths due to mushrooms were reported to US poison control centers through the AAPCC, and 1 death was attributed to mushrooms containing ibotenic acid.[15] The patient who died was a 44-year-old man who ate 6-10 freeze-dried mushrooms, purported to be A muscaria, which he obtained from the Internet. Paramedics found him in cardiac arrest, and he eventually died 10 days later with anoxic brain injury. The report did not mention whether and how the mushroom was confirmed to be A muscaria.

Of the 52 cases of single-substance exposure to ibotenic acid−containing mushrooms reported by US poison control centers through the AAPCC in 2009, 27% had no or minor effects, 37% had moderate effects, 7% had major effects, and 29% had unknown outcomes.[8]

In Slovenia, a 48-year-old man consumed several A muscaria mushrooms and began to experience vomiting and lethargy within 30 minutes.[16] He was found comatose, having a seizurelike episode; he then awoke and was oriented 10 hours after ingestion. By 18 hours after ingestion, the patient’s condition had deteriorated, and he became confused and uncooperative. Paranoid psychosis with visual and auditory hallucinations appeared, persisted for 5 days, and resolved with short-term drug therapy, without any subsequent recurrence.

In Poland, 5 young adults aged 18-21 years consumed dried A muscaria and a can of beer, and 4 of the 5 experienced heightened visual and auditory perceptions beginning about 20 minutes after ingestion.[17] Of these 4, 1 experienced severe hallucinations and lost consciousness, according to the others, who induced vomiting and gave her liquids. The next day, this person came to a hospital complaining of tiredness and gastric pain. She was evaluated, observed for several days, and sent home. No confirmation of the mushrooms was performed.

Also in Poland, 2 women ate 5 fried caps of A pantherina (later confirmed) and developed nausea, stomachache, diarrhea, and vomiting within 2 hours.[18] They subsequently developed ataxia, waxing and waning obtundation, altered perceptions, hyperkinetic movements, and altered speech. One patient’s symptoms lingered for several days, whereas the other had no symptoms at 6 hours after ingestion; the latter received activated charcoal and intravenous (IV) fluids.

In a series of 9 children aged 1-6 years who ingested A muscaria or A pantherina and were treated at a hospital in Seattle, Washington, symptoms developed within 30-180 minutes (median, 45 minutes) after ingestion and lasted for 4-14 hours (median, 9 hours).[12] Symptoms included lethargy (4 children), unresponsiveness (1), comalike sleep (1), ataxia (2), abnormal movements (3), tonic-clonic seizures (3), and agitation, babbling, or hysteria (5). All 9 children recovered uneventfully within 12 hours after admission.

Descriptions of cases reported to the toxicology section of the North American Mycological Association illustrate the typical course of many mushroom poisonings; however, these cases were not necessarily observed by health care professionals.[19]

 

Presentation

History

Obtain a history of the exposure that includes the following:

  • Quantity of mushrooms ingested – The concentration of active substances is low in any individual mushroom, but as a general rule, toxic symptoms result from the consumption of about 1 mushroom by young children and 3 or more by adolescents and adults[13] ; an amount as small as a mouthful can cause symptoms[12]

  • Preparation of the mushroom (eg, raw or cooked) – The effects of mushrooms vary greatly, and cooking may not alter toxicity

  • Source of the mushroom (eg, outdoors or the Internet)

  • Time of ingestion

  • Symptoms seen after ingestion and time between ingestion and onset – Symptoms tend to appear more quickly after ingestion of hallucinogenic mushrooms than after ingestion of more lethal mushrooms

  • Prehospital treatment, including home remedies

  • Medications regularly taken and any co-ingestants

The timing of symptom onset is important for distinguishing life-threatening or severe mushroom poisonings from less serious ones, which typically have an onset of symptoms well within 5 hours of ingestion (as is the case for poisonings involving hallucinogenic mushrooms). If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 hours or more after ingestion, mushrooms that can cause potentially life-threatening or severe toxicity (eg, A phalloides or Cortinarius spp) should be considered.[20, 21, 22, 23, 24]

Note, however, that Amanita smithiana, a mushroom found in the northwestern United States, is characterized by the onset of GI distress within 1-12 hours after ingestion.[25] For mushroom ingestions in the Pacific Northwest, patients who have early-onset symptoms (24</ref>

Identification of the actual mushroom consumed is important but is typically impossible because the mushroom in question has already been digested. (See Identification of Mushroom Specimens.) Collecting the patient’s gastric contents by means of gastric lavage or after emesis might yield identifiable spores. Remote viewing of digital images of an unknown mushroom may facilitate its identification by a mycologist.[26]

For more information on differentiating among various mushroom poisonings, see Mushroom Toxicity.

Mushrooms containing ibotenic acid and muscimol

Symptoms of poisoning with ibotenic acid or muscimol typically begin 30 minutes to 1 hour after ingestion; in rare cases, however, symptom onset may be delayed as long as 3 hours.

Hallucinations may be accompanied by dysarthria, ataxia, and muscle cramps and may persist for as long as 8 hours. However, a case report described an otherwise healthy 48-year-old man who accidentally ingested A muscaria mushrooms and experienced a 5-day paranoid psychosis accompanied by visual and auditory hallucinations.[16] By day 6, his condition had returned to baseline, with no long-term adverse effects reported.

Central nervous system (CNS) effects range from agitation to coma. Heavy intoxication may cause vomiting, diarrhea, and seizures.

Fatal A pantherina poisonings have been reported in the Pacific Northwest region of the United States.[4, 18, 27]

Mushrooms containing psilocybin

Alterations in perception begin within 30 minutes of ingestion of psilocybin-containing mushrooms and generally subside after 6 hours.

Widely varying CNS manifestations (eg, euphoria, visual and religious hallucinations, and feeling closer to nature) have been reported. Visual hallucinations may include perceived motion of stationary objects or surfaces.[28] Patients presenting in the emergency department (ED) may describe more unpleasant effects, such as fear, agitation, confusion, delirium, psychosis, and schizophrenia-like syndromes.

Symptoms may include nausea and sympathomimetic activity such as mydriasis and tachycardia. Symptoms in children include hyperpyrexia and seizures.

Physical Examination

Physical examination typically yields the following findings:

  • Vital signs – Pulse and blood pressure are usually unchanged.

  • Respiration – Breathing is slow and regular, similar to that in deep sleep

  • Gastrointestinal (GI) – GI upset and vomiting occur but are not common; when vomiting or diarrhea does occur, fluid and electrolyte changes are uncommon

  • Integumentary – Skin may be reddened and warm to the touch

  • Musculoskeletal – Muscle spasms may occur

  • Neurologic (eg, ataxia, incoordination, confusion, delirium, and psychosis) – Agitation and CNS depression may occur; especially in children, tonic-clonic seizures, fasciculations, and myoclonic jerking lasting 6-9 hours have been reported[12] ; seizures in adults are uncommon

In these intoxications, neurologic findings predominate. Initial excitation leads to stupor, then coma; severe lethargy alternating with agitation is common, and a deep sleep may occur. Agitation, babbling, confusion, screaming, irritability, hallucinations, dizziness, ataxia, euphoria progressing to muscle jerks, spasms, delirium, racing thoughts, and giddiness may be seen. Headache may last several days. Illusions of sight and sound are produced by misinterpretation of sensory input. Fever, tachycardia, and hypotension may occur because of agitation.

Complications

In addition to CNS sequelae, hallucinogenic mushrooms may affect other organ systems. In one case of psilocybin intoxication, an 18-year-old man developed a cardiac dysrhythmia and myocardial infarction.[29]

Another case report described a 25-year-old man who developed rhabdomyolysis and acute renal failure followed by posterior encephalopathy and cortical blindness after ingesting hallucinogenic mushrooms.[30, 31]

 

DDx

Diagnostic Considerations

In addition to the conditions listed in the differential diagnosis, ingestion of the following mushrooms should be considered:

  • Other Psilocybe spp
  • Amanita cothurnata
  • Amanita smithiana
  • Amanita strobiliformis
  • Amanita gemmata

When other members of the genus Amanita are suspected, the following conditions should be watched for:

  • Ketamine toxicity
  • Meningoencephalitis
  • Dextromethorphan toxicity
  • Gamma-hydroxybutyrate toxicity

Differential Diagnoses

 

Workup

Approach Considerations

No particular diagnostic procedures are available or needed for most patients with toxicity from mushrooms containing muscimol or ibotenic acid.

Laboratory studies can be helpful in identifying complications of hallucinogenic mushroom abuse, which may include hepatotoxicity with repeated use, acute renal failure, and rhabdomyolysis.[31] Serum levels and urine tests for toxins such as muscarine, muscimol, and psilocybin are available but are rarely helpful or necessary in clinical practice.[32] They are more applicable to forensic investigations.

Identification of the mushroom by a mycologist is desirable. Gastric contents may be examined. A mycologist may be able to microscopically identify the spores recovered from the patient’s gastric contents.

Laboratory Studies

A complete blood count (CBC) should be obtained because some mushroom toxins (eg, gyromitrin) can cause hemolytic anemia.

Baseline liver function studies are indicated because possible ingestion of other toxic mushrooms (eg, those containing cyclopeptides) can cause hepatotoxicity.

Baseline renal function studies are indicated because some mushrooms are nephrotoxic, such as A smithiana and orelline mushrooms.

Evaluation for rhabdomyolysis should be considered if signs and symptoms warrant because some mushrooms (eg, Tricholoma equestre) may cause muscle toxicity.

A basic serum metabolic profile (sodium, potassium, chlorine, carbon dioxide, creatinine, glucose, and calcium) should be obtained to evaluate for fluid and electrolyte disturbances due to other offending ingestants.

Urine drug screening should be considered, especially if the patient has unexplained symptoms or behavioral changes, if suicidal intent, substance abuse or foul play is suspected, or if ingestion of unknown toxins is suspected. The patient’s urine may be analyzed for muscimol to confirm muscimol poisoning, but this test is not typically available in hospital laboratories.

Identification of Mushroom Specimens

Identification of the mushroom ingested is generally desirable. However, with hallucinogenic mushrooms, definitive identification is seldom necessary. Exact identification of the mushroom is achieved in fewer than 3% of cases.

Mushrooms in the ibotenic acid group (see the images below) are commonly found throughout the United States, Europe, and Asia. They are found in wooded areas, especially among conifer forests, in the spring and fall seasons of North America. The young specimens emerge with patches of membrane left covering the cap and forming a cup (volva) at the base. The mature specimens often have brilliant cap colors and delicate skirts and cups.

Fly agaric (Amanita muscaria). Fly agaric (Amanita muscaria).
Amanita muscaria. Amanita muscaria.
Amanita muscaria var. guessowii with yellow cap su Amanita muscaria var. guessowii with yellow cap surface, from Massachusetts.
Amanita muscaria var. formosa sensu Thiers, from O Amanita muscaria var. formosa sensu Thiers, from Oregon.
Amanita pantherina. Amanita pantherina.

A muscaria can occur alone or in groups on the ground of forests, in grassy areas and lawns, and especially under trees. The cap is 5-30 cm in diameter and contains white warts. The stalk is white, frequently hollow, and often as long as 15-20 cm. A prominent volva is found at the bottom of the stalk, with numerous rings superiorly. The gills are free and white. The spores are also white. The appearance varies according to geographic location. Scarlet caps are most common in western North America, orange to yellow-orange caps in eastern North America.

Different types of mushrooms can be found in the same location, and reliance on a single sample can lead to false identification of the mushroom that was ingested. All mushrooms in the immediate vicinity of the ingestion site must be considered. When no specimen is brought in by a patient with a suspected mushroom ingestion, sending an experienced forager to the site to collect any mushrooms growing in the area might be helpful.

When mushroom specimens are obtained for identification, the entire mushroom should be dug up to preserve the architecture of the bulb, stem, and cap. (Keep in mind, however, that definitive identification should be made by an experienced mycologist rather than by a physician.)

To make a spore print, slice the mushroom stem from the cap very close to the gills, and lay the cap onto a piece of paper with the gills down. Make prints on black-and-white paper. These can be sent to the regional poison control center or its designee for analysis.

Whole mushrooms can be sent. Samples should include, if possible, the deeply rooted portion of the fungus, as well as the cap and gills. They should not be packaged in plastic or cloth, because they may decompose rapidly. Samples should be placed in a paper bag with an absorbant (eg, a piece of filter paper) to prevent condensation. Transporting the mushrooms in this way minimizes destruction of their natural architecture, discoloration of the cap or gills, and premature release of the spores. The mushrooms also must not be refrigerated or crushed.

The widespread availability of digital cameras enables rapid transmission of images of mushroom samples to mycologists over the Internet. Although it may not be possible to make a definitive identification via this method, it may be possible at least to rule out certain species.[26]

Other Studies

Chromatographic techniques (eg, thin-layer chromatography [TLC], gas-liquid chromatography [GLC], and high-pressure liquid chromatography [HPLC]) are available to detect ibotenic acid, muscimol,[33] and psilocybin, as well as other mushroom toxins (eg, amanitins, orellanine, muscarine, and gyromitrins). However, these techniques are typically unavailable to general practitioners, being largely restricted to laboratories conducting research on these compounds.

If the diagnosis is uncertain, and if blunt head trauma is part of the differential diagnosis because of changes in mental status, plain computed tomography (CT) of the head is warranted before lumbar puncture is performed.

 

Treatment

Approach Considerations

Prehospital care is primarily supportive, with appropriate attention paid to the ABCs (airway, breathing, circulation). Emergency department (ED) care is primarily supportive as well.[34]

The entire poisoning episode usually subsides in 6-8 hours; some symptoms may take up to several days to fully resolve. Benzodiazepines may be used for sedation and treatment of panic attacks, hallucinations, and seizures. Psychiatric consultation and evaluation may be needed for persistent psychotic symptoms.[1]

 

 

Supportive Measures

Symptomatic patients may be treated with supportive measures, including the following:

  • Consider gastric lavage if ingestion occurred within approximately 1 hour of presentation (though there are no data to support the efficacy of the procedure in this setting)

  • Consider oral administration of activated charcoal if the patient presents within 1 hour of ingestion[35] ; however, adsorption to activated charcoal has not been demonstrated for these constituents,[36] and there is no evidence that routine administration of multiple doses of activated charcoal is useful

  • Consider administering intravenous (IV) fluids if vomiting becomes prominent (a rare occurrence) or signs of volume depletion are present

  • Provide agitated patients with a quiet, nonthreatening environment.

  • Provide psychiatric care to patients with intentional ingestions and suicidal thinking

With good supportive care, most patients recover within 6-8 hours and may be discharged from the ED at that time, provided no complicating issues are present and they have a safe environment to which to return.

 

Pharmacologic Therapy

Most patients with poisoning due to ibotenic acid−containing mushrooms can be treated without medications. If patients are severely agitated, anxiolytics (eg, benzodiazepines) may be needed. For seizures lasting longer than 5 minutes, various anticonvulsants have been used. It should be kept in mind that respiratory depression has been reported when these agents are administered IV. Preparations must therefore be made to support the airway if necessary.[13]

Ipecac syrup should generally be avoided. Central nervous system (CNS) symptoms develop relatively rapidly after ingestion of ibotenic acid−containing mushrooms, and evidence for the effectiveness of ipecac in this setting is lacking.

With A muscaria poisoning, despite the implications of the species name, few muscarinic effects are observed; consequently, anticholinergic drugs such as atropine are rarely, if ever, needed.

Fever in this setting should not be treated with antipyretics; it is probably the result of agitation and increased motor activity.

Prevention

Cautious mushroom hunters eat only 1 type of mushroom and save a sample in a dry paper bag for later identification, if needed. Identification of mushrooms is best left to experts. Prevention is achieved by eating only mushrooms that are commercially cultivated for human consumption. Mushrooms should be regularly removed from sites where children are routinely present.

Consultations

A mycologist should be consulted to assist with mushroom identification. The regional poison control center may be contacted for consultation, referral, and, if necessary, assistance in mushroom identification. A nationwide telephone number, 1-800-222-1222, is available in the United States; calls to this number are automatically directed to the nearest poison control center. A mycologist can also be contacted through a mycology club, the North American Mycological Association (NAMA), a botanical garden, or a local university.

Consultation with a medical toxicologist may be helpful, if available. Consultation with a psychiatrist is advisable when the patient may have had suicidal intent.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to neutralize the mushroom toxin (ibotenic acid, muscimol, psilocybin, or psilocin). Agents used include gastrointestinal (GI) decontaminants and benzodiazepines.

GI decontaminants

Class Summary

Activated charcoal is preferred when GI decontamination is desired.

Activated charcoal (Liqui-Char)

Activated charcoal is most useful if administered within 2 hours of ingestion. Outcome data are limited, especially when the agent is given more than 1 hour after ingestion. Administration of charcoal by itself (in aqueous solution), as opposed to coadministration with a cathartic, is the current practice standard for the following reasons:

• No studies have shown benefit from cathartics in this setting

• Whereas most drugs and toxins are adsorbed within 30-90 minutes, laxatives take hours to work

• Dangerous fluid and electrolyte shifts have occurred when cathartics are used in small children

When the ingested dose is known, charcoal may be given at 10 times the ingested dose in either 1 or 2 doses. For maximum effect, administer within 30 minutes of poison ingestion.

Benzodiazepines

Class Summary

Benzodiazepines are first-line agents for preventing seizure recurrence and terminating clinical and electrical seizure activity in patients with toxicity. They are also helpful in sedating patients with extreme agitation.

Diazepam (Valium)

Diazepam depresses all levels of the central nervous system (CNS), including the limbic system and the reticular formation, possibly by increasing the activity of gamma-aminobutyric acid (GABA). To avoid adverse effects, individualize the dosage and increase it cautiously.

Lorazepam (Ativan)

Lorazepam is useful for agitation or seizures and is the drug of choice for treatment of status epilepticus (because it persists in the CNS longer than diazepam does). By increasing the action of GABA (a major inhibitory neurotransmitter in the brain), it may depress all levels of the CNS, including the limbic system and the reticular formation. The rate of injection should not exceed 2 mg/min. Lorazepam may be administered intramuscularly (IM) if vascular access cannot be obtained.

Midazolam (Versed)

Midazolam is used as an alternative for terminating refractory status epilepticus. Because it is water-soluble, it takes approximately 3 times longer to achieve peak electroencephalographic (EEG) effects than diazepam does. Thus, the clinician must wait 2-3 minutes to evaluate its sedative effects fully before initiating a procedure or repeating the dose. Midazolam has twice the affinity for benzodiazepine receptors that diazepam does. It may be administered IM if vascular access cannot be obtained.